A number of studies have showed that recently created genes
differ from the genes created in deep evolutionary past in many
aspects. Here, we determined the age of emergence and propensity
for gene loss (PGL) of all human protein-coding genes and compared
disease genes with non-disease genes in terms of their evolutionary
rate, strength of purifying selection, mRNA expression, and genetic
redundancy. The older and the less prone to loss, non-disease genes
have been evolving 1.5- to 3-fold slower between humans and chimps
than young non-disease genes, whereas Mendelian disease genes have
been evolving very slowly regardless of their ages and PGL. Complex
disease genes showed an intermediate pattern. Disease genes also
have higher mRNA expression heterogeneity across multiple tissues
than non-disease genes regardless of age and PGL. Young and
middle-aged disease genes have fewer similar paralogs as
non-disease genes of the same age. We reasoned that genes were more
likely to be involved in human disease if they were under a strong
functional constraint, expressed heterogeneously across tissues,
and lacked genetic redundancy. Young human genes that have been
evolving under strong constraint between humans and chimps might
also be enriched for genes that encode important primate or even
human-specific functions.